Mutants resistant to the methionine analog ethionine have been isolated. Three types of mutants have been identified. One type (metT) is deficient in methionine and ethionine uptake, another is deficient in S-adenosyl-methionine (SAM) synthetase, and the third (eth) has an unknown biochemical lesion that enables ethionine to increase the frequency at which cells spontaneously enter sporulation. The 2-3% SAM-synthetase activity produced by the metE mutants suffices to enable SAM synthesis and growth at almost the normal rate. The metE double mutants are more resistant to ethionine than either mutant alone, and they no longer sporulate at increased frequency upon ethionine addition. Apparently, this increased sporulation is due to the synthesis of S-adenosyl-ethionine, which has been identified by HPLC. In the eth mutant, DNA sites which can be specifically cut by the hsrR restriction endonuclease, are more methylated than in the standard strain. This was shown by the restriction pattern of phi105 phages grown in these strains.